Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clinical and electrocardiographic findings were analyzed in 100 consecutive cases of LAD. Below the age of forty years, LAD was uncommon, but its incidence increased continuously thereafter. The most frequent primary clinical diagnosis was arteriosclerotic heart disease. The functional mechanism producing LAD most often was LAHB, responsible in about 40 per cent. Approximately half the instances of LAHB were associated with old myocardial infarction of septal, anterior, or lateral regions, but half were seen in the absence of infarction or clinical coronary sclerosis and are presumed due to primary degenerative processes within these specialized conducting fibers. Approximately one-sixth of the instances of LAD were due to loss of inferior forces following inferior myocardial infarction. Typical left ventricular hypertrophy was a distinctly uncommon cause of LAD. Last, in 24 patients with LAD the mechanism or cause was not evident initially, of which two were subsequently shown to represent a very mild degree of LAHB. Also it is suggested that asymmetric myocardial hypertrophy of the anterior wall may account for some instances of LAD not otherwise explained.
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PMID:Left-axis deviation: etiologic factors in one-hundred patients. 111 74

A 66-year-old man, who had atrial septal defect (ASD) associated with severe coronary artery disease, underwent closure of ASD and concomitant coronary artery bypass grafting (LIMA-LAD & SVG-RCA). Response to surgery was excellent, with improvement of cardiac function and returning to NYHA functional class I, while, preoperatively, the patient had been limited due to symptoms related both to large left to right shunt flows (Qp/Qs 3.04) and to left ventricular dysfunction because of severe myocardial ischemia as well as previous inferior myocardial infarction. SAD is the most common form of congenital heart disease requiring surgery in adults, accordingly it should be remembered that some of the elderly patients with ASD might have obvious or occult coronary artery disease at the time of diagnosis and operative intervention.
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PMID:[A case of successful surgery of atrial septal defect combined with coronary artery bypass grafting]. 278 42

Implantation of a transvenous device in patients with a tricuspid valve replacement or a complex congenital heart disease with no access to the right ventricle represents problems. The lack of access to the right ventricle might preclude transvenous placement of a defibrillation lead at ICD implantation. A young patient (21 years) with a history of severe chest trauma with rupture of the tricuspid valve as well as the right coronary artery and consecutive inferior myocardial infarction was initially treated with tricuspid valve replacement (St Jude Medical artificial prosthesis, 33 mm) and a bypass graft to the right coronary artery. Four years later, the patient was admitted with a hemodynamically not tolerated ventricular tachycardia (VT: CL 250 ms, LBBB, left axis). The VT could be reproduced during electrophysiological testing. An ICD was implanted subpectorally in combination with a transvenous active fixation ICD lead. The transvenous ICD lead was placed via a guiding catheter into a coronary sinus branch (middle cardiac vein). Acceptable pacing and sensing values could be obtained. The defibrillation threshold was 25 J. In conclusion transvenous ICD lead implantation into a side branch of the coronary sinus in combination with a pectorally implanted "active can" ICD device seems to be an alternative approach. This approach may avoid implantation of additional subcutaneous defibrillation leads or even thoracotomy for ICD implantation.
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PMID:Transvenous ICD implantation after artificial tricuspid valve replacement. A new approach placing a transvenous ICD lead in the mid cardiac vein of the coronary sinus. 1614 19

The J wave syndrome is characterized by a prominent J wave accompanied by ST-segment elevation in the absence of structural heart disease. It includes the benign early repolarization syndrome, the highly arrhythmogenic Brugada syndrome and idiopathic ventricular fibrillation. Although acute coronary syndromes are one of the leading causes of ST-segment deviation, no clinical reports that specifically describe the modulating effects of an ischemic injury current on the ECG manifestations of the J wave syndrome have been found. This report describes four cases of patients with acute inferior ST-segment elevation myocardial infarction who had J wave (or negative deplacement of the J point) and ST-segment depression in the right precordial leads. Later, these precordial ECG alterations disappeared and were progressively replaced by prominent J (R') waves and anterior ST-segment elevations, suggesting the presence of a J wave syndrome. In conclusion, the J wave syndrome may be obscured by an acute inferior myocardial infarction with concomitant ST-segment depression in the right precordial leads. In such circumstances, early detection of the J wave (or depressed J point) may be used as ECG marker of the early repolarization syndrome or Brugada syndrome.
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PMID:[Acute inferior myocardial infarction masking the J wave syndrome. Based on four observations]. 1822 13

The so-called 'masquerading' type of right bundle branch block is caused by the simultaneous presence of a high-degree left anterior fascicular block often accompanied with severe left ventricular enlargement and/or fibrotic block in the anterolateral wall of the left ventricle. These conditions tend to reorient the terminal electrical forces of the QRS complex towards the left and upwards, in such a way that the characteristic slurred S wave in lead I becomes smaller or even disappears. In many cases of standard masquerading right bundle branch block, a small Q wave in lead I is present due to the initial forces of the left anterior fascicular block, which are oriented rightwards and inferiorly. However, in some cases, the Q wave in lead I also vanishes, and the mimicking of a left bundle branch block becomes perfect in standard leads. This is commonly associated with an inferior myocardial infarction or severe inferior fibrosis in cardiomyopathies. The typical QRS changes of right bundle branch block may eventually be concealed even in the right precordial leads; under such circumstances, the ECG diagnosis may be mistaken and the right bundle branch block totally missed. The masquerading right bundle branch block carries a poor prognosis, since it always implies the presence of a severe underlying heart disease.
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PMID:Masquerading bundle branch block: a variety of right bundle branch block with left anterior fascicular block. 2325 47